Acute Myocardial Infarction and Stress Cardiomyopathy Are Not Mutually Exclusive
Iliana S Hurtado Rendón1, Diego Alcivar1, Juan Pablo Rodriguez-Escudero1
1Department of Cardiology, Summa Cardiovascular Institute, Summa Health, Akron, Ohio.
Insights
Acute coronary syndrome can trigger stress cardiomyopathy, a condition with temporary heart dysfunction. This study shows stress cardiomyopathy may arise from acute myocardial infarction, resolving without intervention.
Area of Science:
- Cardiology
- Internal Medicine
Background:
- Stress cardiomyopathy is a transient cardiac syndrome with reversible left ventricular systolic dysfunction.
- It is often precipitated by emotional or physiologic stress and can coexist with obstructive coronary artery disease.
Observation:
- Three cases of acute coronary syndrome (ACS) presented with transient wall motion abnormalities.
- These abnormalities were not typically observed in the coronary artery disease distribution.
Findings:
- In acute myocardial infarction cases, coronary occlusion distribution did not match transient wall motion abnormality territories.
- Wall motion abnormalities resolved spontaneously without intervention in follow-up.
Implications:
- Physiologic stress from ACS may precipitate stress cardiomyopathy.
- This suggests a novel pathway where acute coronary syndrome can trigger stress cardiomyopathy.
Background:
Stress cardiomyopathy is a transient cardiac syndrome characterized by reversible left ventricular systolic dysfunction precipitated by emotional or physiologic stress. The presence of obstructive coronary artery disease has been noted in stress cardiomyopathy.
Methods:
We describe 3 case reports of patients with acute coronary syndrome and transient wall motion abnormalities not usually seen in the distribution of coronary artery disease.
Results:
In these 3 cases of acute myocardial infarction, the distribution of the culprit coronary occlusion was not concordant with the territory of transient wall motion abnormality. Follow-up demonstrated resolution of the wall motion abnormalities without intervention in these territories.
Conclusion:
We believe that the physiologic stress of the acute coronary syndrome may have precipitated the stress cardiomyopathy as presented by these patients. This is the first demonstration that stress cardiomyopathy may be precipitated by acute coronary syndrome.
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